| Summary: | This study was aimed to explore the role of tanshinol in osteoblastic cells, and the role in vivo using an ovariectomized (OVX) rat model of osteoporosis. MC3T3-E1 cells were pretreated with 0-400 μg/mL tanshinol, and then cell viability, apoptosis, alkaline phosphatase (ALP) activity and the expressions of Collagen Type I Alpha 1 (Col1A1), Runt Related Transcription Factor 2 (Runx2) and osteocalcin (OCN) were respectively detected. Rats underwent OVX surgery was intervened with 5 mg/kg tanshinol or 25 μg/kg β-estradiol (E2) for 12 weeks. The triglycerides (TG), total cholesterol (TC), high and low density lipoprotein cholesterol (HDL-C and LDL-C), ALP, OCN and Tartrate-resistant acid phosphatase-5b (TRACP-5b) contents were measured. Besides, the expressions of main factors in nuclear factor-kappa B (NF-κB) pathway were detected. The results showed that tanshinol significantly promoted MC3T3-E1 cells viability and ALP activity, while inhibited apoptosis (P < 0.05); Col1A1, Runx2 and OCN were all up-regulated by tanshinol (P < 0.05). In OVX rats, the contents of TG, TC, LDL-C, ALP, OCN and TRACP-5b were all increased (P < 0.05), while HDL-C was decreased (P < 0.05). Tanshinol significantly alleviated these aberrant regulations (P < 0.05). Inhibitory subunit of NF-κB (IκBα) and p65 were both remarkably phosphorylated by OVX, while this phosphorylation was partially neutralized by tanshinol (P < 0.05). In conclusion, we demonstrated that tanshinol exerted a bone-protective function by modulating the markers of bone turnover possibly via blocking NF-κB pathway. This study will provide new evidence that tanshinol is a potential therapeutic option for the relief of estrogen deficiency-induced osteoporosis.
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